scholarly journals TWE-PRIL reverse signalling suppresses sympathetic axon growth and tissue innervation

Development ◽  
2018 ◽  
Vol 145 (22) ◽  
pp. dev165936 ◽  
Author(s):  
Laura Howard ◽  
Erin Wosnitzka ◽  
Darian Okakpu ◽  
Matthew A. White ◽  
Sean Wyatt ◽  
...  
Keyword(s):  
Axon Growth ◽  
Sympathetic Axon

Vascular-derived artemin: a determinant of vascular sympathetic innervation?

2007 ◽  
Vol 293 (1) ◽  
pp. H266-H273 ◽  
Author(s):  
Deborah H. Damon ◽  
Jaclyn A. teRiele ◽  
Stephen B. Marko
Keyword(s):  
Important Determinant ◽  
Sympathetic Neurons ◽  
Sympathetic Innervation ◽  
Axon Growth ◽  
Neurite Growth ◽  
Sympathetic Ganglia ◽  
Neonatal Rat ◽  
Rt Pcr ◽  
Adult Rats ◽  
Sympathetic Axon

Vascular sympathetic innervation is an important determinant of blood pressure and blood flow. The mechanisms that determine vascular sympathetic innervation are not well understood. The present study tests the hypothesis that vascular-derived artemin promotes the development of sympathetic innervation to blood vessels by promoting sympathetic axon growth. RT-PCR and Western analyses indicate that artemin is expressed by cultured vascular smooth muscle and arteries, and artemin coreceptors, glial cell-derived neurotrophic factor family receptor α3 and ret, are expressed by postganglionic sympathetic neurons. The effects of artemin on axon growth were assessed on explants of neonatal rat sympathetic ganglia. In the presence, but not in the absence, of nerve growth factor, exogenous artemin stimulated neurite growth. Femoral arteries (FA) from adult rats contain artemin, and these arteries stimulated sympathetic neurite growth. Growth in the presence of FA was 92.2 ± 11.9 mm, and that in the absence of FA was 26.3 ± 5.4 mm ( P < 0.05). FA stimulation of axon growth was reduced by an antibody that neutralized the activity of artemin ( P < 0.05). These data indicate that artemin is expressed in arteries, and its receptors are expressed and functional in the postganglionic sympathetic neurons that innervate them. This suggests that artemin may be a determinant of vascular sympathetic innervation.

scholarly journals T-type Ca 2+ channels are required for enhanced sympathetic axon growth by TNFα reverse signalling

Open Biology ◽  
2017 ◽  
Vol 7 (1) ◽  
pp. 160288 ◽  
Author(s):  
Lilian Kisiswa ◽  
Clara Erice ◽  
Laurent Ferron ◽  
Sean Wyatt ◽  
Catarina Osório ◽  
...  
Keyword(s):  
Sympathetic Neurons ◽  
Sympathetic Innervation ◽  
Axon Growth ◽  
Tumour Necrosis Factor Receptor ◽  
Kinase C ◽  
Cultured Sympathetic Neurons ◽  
Sympathetic Axon ◽  
Pkc Activation ◽  
Cell Somata ◽  
Necrosis Factor

Tumour necrosis factor receptor 1 (TNFR1)-activated TNFα reverse signalling, in which membrane-integrated TNFα functions as a receptor for TNFR1, enhances axon growth from developing sympathetic neurons and plays a crucial role in establishing sympathetic innervation. Here, we have investigated the link between TNFα reverse signalling and axon growth in cultured sympathetic neurons. TNFR1-activated TNFα reverse signalling promotes Ca 2+ influx, and highly selective T-type Ca 2+ channel inhibitors, but not pharmacological inhibitors of L-type, N-type and P/Q-type Ca 2+ channels, prevented enhanced axon growth. T-type Ca 2+ channel-specific inhibitors eliminated Ca 2+ spikes promoted by TNFα reverse signalling in axons and prevented enhanced axon growth when applied locally to axons, but not when applied to cell somata. Blocking action potential generation did not affect the effect of TNFα reverse signalling on axon growth, suggesting that propagated action potentials are not required for enhanced axon growth. TNFα reverse signalling enhanced protein kinase C (PKC) activation, and pharmacological inhibition of PKC prevented the axon growth response. These results suggest that TNFα reverse signalling promotes opening of T-type Ca 2+ channels along sympathetic axons, which is required for enhanced axon growth.

Vascular endothelial-derived semaphorin 3 inhibits sympathetic axon growth

2006 ◽  
Vol 290 (3) ◽  
pp. H1220-H1225 ◽  
Author(s):  
Deborah H. Damon
Keyword(s):  
Axon Guidance ◽  
Vascular Endothelial Cells ◽  
Sympathetic Innervation ◽  
Axon Growth ◽  
Sympathetic Ganglia ◽  
Vascular Endothelial ◽  
Semaphorin 3A ◽  
Rt Pcr ◽  
Guidance Cue ◽  
Sympathetic Axon

Vascular sympathetic innervation is an important determinant of blood pressure and blood flow. The mechanisms that determine vascular sympathetic innervation are not well understood. Recent studies indicate that vascular endothelial cells (EC) express semaphorin 3A, a repulsive axon guidance cue. This suggests that EC would inhibit the growth of axons to blood vessels. The present study tests this hypothesis. RT-PCR and Western analyses confirmed that rat aortic vascular ECs expressed semaphorin 3A as well as other class 3 semaphorins (sema 3s). To determine the effects of EC-derived sema 3 on sympathetic axons, axon outgrowth was assessed in cultures of neonatal sympathetic ganglia grown for 72 h in the absence and presence of vascular EC. Nerve growth factor-induced axon growth in the presence of ECs was 50 ± 4% ( P < 0.05) of growth in the absence of ECs. ECs did not inhibit axon growth in the presence of an antibody that neutralized the activity of sema 3 ( P > 0.05). RT-PCR and Western analyses also indicated that sema 3s were expressed in ECs of intact arteries. To assess the function of sema 3s in arteries, sympathetic ganglia were grown in the presence of arteries for 72 h, and the percentage of axons that grew toward the artery was determined: 44 ± 4% of axons grew toward neonatal carotid arteries. Neutralization of sema 3s or removal of EC increased the percentage of axons that grew toward the artery (71 ± 8% and 72 ± 8%, respectively). These data indicate that vascular EC-derived sema 3s inhibit sympathetic axon growth and may thus be a determinant of vascular sympathetic innervation.

scholarly journals TNFα reverse signaling promotes sympathetic axon growth and target innervation

2013 ◽  
Vol 16 (7) ◽  
pp. 865-873 ◽  
Author(s):  
Lilian Kisiswa ◽  
Catarina Osório ◽  
Clara Erice ◽  
Thomas Vizard ◽  
Sean Wyatt ◽  
...  
Keyword(s):  
Axon Growth ◽  
Reverse Signaling ◽  
Target Innervation ◽  
Sympathetic Axon

scholarly journals CD40L reverse signaling suppresses prevertebral sympathetic axon growth and tissue innervation

2019 ◽  
Vol 79 (11-12) ◽  
pp. 949-962
Author(s):  
Osman Yipkin Calhan ◽  
Sean Wyatt ◽  
Alun Millward Davies
Keyword(s):  
Axon Growth ◽  
Reverse Signaling ◽  
Sympathetic Axon

The metalloproteinase ADAM10 is required for retinal ganglion cell axon guidance in the developing visual systems

2007 ◽  
Vol 30 (4) ◽  
pp. 77
Author(s):  
Y. Y. Chen ◽  
C. L. Hehr ◽  
K. Atkinson-Leadbeater ◽  
J. C. Hocking ◽  
S. McFarlane
Keyword(s):  
Ganglion Cell ◽  
Axon Guidance ◽  
Retinal Ganglion Cell ◽  
Growth Cone ◽  
Expression Patterns ◽  
Optic Tract ◽  
Axon Growth ◽  
Proteolytic Processing ◽  
Retinal Ganglion

Background: The growth cone interprets cues in its environment in order to reach its target. We want to identify molecules that regulate growth cone behaviour in the developing embryo. We investigated the role of A disintegrin and metalloproteinase 10 (ADAM10) in axon guidance in the developing visual system of African frog, Xenopus laevis. Methods: We first examined the expression patterns of adam10 mRNA by in situ hybridization. We then exposed the developing optic tract to an ADAM10 inhibitor, GI254023X, in vivo. Lastly, we inhibited ADAM10 function in diencephalic neuroepithelial cells (through which retinal ganglion cell (RGC) axons extend) or RGCs by electroporating or transfecting an ADAM10 dominant negative (dn-adam10). Results: We show that adam10 mRNA is expressed in the dorsal neuroepithelium over the time RGC axons extend towards their target, the optic tectum. Second, pharmacological inhibition of ADAM10 in an in vivo exposed brain preparation causes the failure of RGC axons to recognize their target at low concentrations (0.5, 1 μM), and the failure of the axons to make a caudal turn in the mid-diencephalon at higher concentration (5 μM). Thus, ADAM10 function is required for RGC axon guidance at two key guidance decisions. Finally, molecular inhibition of ADAM10 function by electroporating dn-adam10 in the brain neuroepithelium causes defects in RGC axon target recognition (57%) and/or defects in caudal turn (12%), as seen with the pharmacological inhibitor. In contrast, molecular inhibition of ADAM10 within the RGC axons has no effect. Conclusions: These data argue strongly that ADAM10 acts cell non-autonomously within the neuroepithelium to regulate the guidance of RGC axons. This study shows for the first time that a metalloproteinase acts in a cell non-autonomous fashion to direct vertebrate axon growth. It will provide important insights into candidate molecules that could be used to reform nerve connections if destroyed because of injury or disease. References Hattori M, Osterfield M, Flanagan JG. Regulated cleavage of a contact-mediated axon repellent. Science 2000; 289(5483):1360-5. Janes PW, Saha N, Barton WA, Kolev MV, Wimmer-Kleikamp SH, Nievergall E, Blobel CP, Himanen JP, Lackmann M, Nikolov DB. Adam meets Eph: an ADAM substrate recognition module acts as a molecular switch for ephrin cleavage in trans. Cell 2005; 123(2):291-304. Pan D, Rubin GM. Kuzbanian controls proteolytic processing of Notch and mediates lateral inhibition during Drosophila and vertebrate neurogenesis. Cell 1997; 90(2):271-80.

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